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Death Receptor 5 Antisense Long Noncoding RNA and Cisplatin Modulate Macromolecular and Metabolic Changes in HeLa Cells

ABSTRACT: We have performed a transcriptomics study in which we first apply cisplatin to HeLa cells. Total RNA was isolated from control as well as treated cells and apoptosis was confirmed by Annexin V and 7AAD staining in flow cytometry. Total RNAs were subjected to deep-sequencing to identify differentially expressed mRNAs. We then took advantage of bioinformatic tools to identify which pathways are affected by Cisplatin treatment

ORGANISM(S): Homo sapiens

PROVIDER: GSE193447 | GEO | 2024/01/17

REPOSITORIES: GEO

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A transcriptomics approach identifies DR5-AS as a cisplatin-inducible long non-coding RNA that modulates cell cycle and proliferation

Project description:We have performed a transcriptomics study in which we first applied 80 uM of cisplatin for 16h. Total RNA was isolated from control as well as drug treated cells and apoptosis induction was confirmed by Annexin V and 7AAD staining. Total RNAs were subjected to deep-sequencing to identify differentially expressed RNAs. We then took advantage of bioinformatic tools to identify which lncRNAs are differentially expressed upon cisplatin treatment

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Knockdown of death receptor 5 antisense long noncoding RNA and cisplatin treatment modulate similar macromolecular and metabolic changes in HeLa cells.

Project description:Background/aimDespite great progress in complex gene regulatory mechanisms in the dynamic tumor microenvironment, the potential contribution of long noncoding RNAs (lncRNAs) to cancer cell metabolism is poorly understood. Death receptor 5 antisense (DR5-AS) is a cisplatin inducible lncRNA whose knockdown modulates cell morphology. However, its effect on cell metabolism is unknown. The aim of this study is to examine metabolic changes modulated by cisplatin and DR5-AS lncRNA in HeLa cells.Materials and methodsWe used cisplatin as a universal cancer therapeutic drug to modulate metabolic changes in HeLa cervix cancer cells. We then examined the extent of metabolic changes by Fourier transform infrared spectroscopy (FTIR). We also performed transcriptomics analyses by generating new RNA-seq data with total RNAs isolated from cisplatin-treated HeLa cells. Then, we compared cisplatin-mediated transcriptomics and macromolecular changes with those mediated by DR5-AS knockdown.ResultsCisplatin treatment caused changes in the unsaturated fatty acid and lipid-to-protein ratios and the glycogen content. These observations in altered cellular metabolism were supported by transcriptomics analyses. FTIR spectroscopy analyses have revealed that DR5-AS knockdown causes a 20.9% elevation in the lipid/protein ratio and a 76.6% decrease in lipid peroxidation. Furthermore, we detected a 3.42% increase in the chain length of the aliphatic lipids, a higher content of RNA, and a lower amount of glycogen indicating relatively lower metabolic activity in the DR5-AS knockdown HeLa cells. Interestingly, we observed a similar gene expression pattern under cisplatin treatment and DR5-AS knockdown HeLa cells.ConclusionThese results suggest that DR5-AS lncRNA appears to account for a fraction of cisplatin-mediated macromolecular and metabolic changes in HeLa cervix cancer cells.

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Dynamic response of annexin A11-associated gene expression to cisplatin treatment

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Death Receptor 5 Antisense Long Noncoding RNA and Cisplatin Modulate Macromolecular and Metabolic Changes in HeLa Cells

Project description:Death Receptor 5 Antisense Long Noncoding RNA and Cisplatin Modulate Macromolecular and Metabolic Changes in HeLa Cells

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Cisplatin-inducible death receptor 5 antisense long non-coding RNA modulates cell cycle and proliferation in HeLa cells

Project description:We have performed a transcriptomics study in which we first transfected LNA GapmeRs against DR5-AS lncRNA to silence it in HeLa cells. Total RNA was isolated from control as well as transfected cells and silencing was confirmed by qPCR. Total RNAs were subjected to deep-sequencing to identify differentially expressed mRNAs. We then took advantage of bioinformatic tools to identify which pathways are affected by DR5-AS knock-down.

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Genomewide m6A mapping uncovers dynamic changes in the m6A epitranscriptome of cisplatin-treated apoptotic HeLa cells

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